Exposure of human skin to sunlight has several known unpleasant effects such as sunburn and pathological lesions leading to carcinogenesis. Due to the ultraviolet radiation of sunlight, free radicals (e.g. hydroxy radicals or nascent oxygen) form in the skin. Such free radicals can injure the DNA of skin cells and contribute to photoaging of the skin.
Photoaging is characterized by clinical, histological and biochemical changes which differ from alterations in chronologically aged but sunprotected skin [Herschenfeld, R. E. et al.: The cumulative effect of ultraviolet radiation on the skin photoaging, in Photodermatology, Hawk, J. L. M. , Ed., Arnold, London, Sydney, Oakland, 1999, 89-102]. Photoaging includes changes attributable to chronic sun exposure and results in dry skin, wrinkling, laxity or even a variety of benign neoplasms.
Free radicals having a powerful oxidizing effect can injure the membrane of cells by oxidizing the unsaturated fatty acid components of the membrane (peroxidization of lipids). Also, reactive aldehydes are formed during the oxidization. In the injury of the membrane, increased intake of calcium leads to cell death, and pathological processes are started due to the presence of the reactive aldehydes:                injury of DNA, resulting in mutation in both the cell nucleus and mitochondria;        changes in the properties of the interstitial proteins (i.e. elastin) owing to the formation of crosslinks.        
It is known that the elastic structures of collagen proteins and elastin contain a lot of water. It is characteristic of the interstitial proteins that they are rich in lysine. The reactive aldehydes such as malondialdehyde result in condensation reactions with the protein side chains containing amino groups to yield crosslinks. Thus, the originally elastic structure of the skin becomes rigid and hydrophobic. During the above process, at first lipofuscin ceroids, then age pigments are formed.
The natural protective mechanism against UV radiation include bronzing due to the formation of melanin, DNA repair mechanisms, etc. Deficiency of a protective mechanism such as DNA repair, with consequent loss of the correction of the DNA injuries caused by UV radiation leads to early photoaging of the skin. Xeroderma pigmentosum is a disease characterized by deficiency of DNA repair that can be accompanied by the development of a malignant tumor. Sunburn spots caused by bronzing in early childhood are photodamage that heals, leaving an extended scar that can result in spinocellular carcinoma or even in various malignant tumors (e.g. melanoma, cerato-acanthoma, basalioma, sarcoma).
Thus, UV radiation-induced injury to the skin can be subdivided into acute photodamage (e.g. sunburn) and chronic photodamage (e.g. photoaging, actinic keratosis, and, ultimately, skin cancers).
Actinic keratosis is a common sun-induced precancerous neoplasm confined to the epidermis. It is the initial manifestation of a continuum of clinical and histologic abnormalities that progresses to invasive squamous cell carcinoma, a disorder that accounts for thousands of death in the USA each year. [Schwartz, R. A.: The Actinic Keratosis, Dermatol. Surg., 23, 1009-1019 (1997).]
Actinic keratosis has been known by a variety of names, including solar keratosis, senile keratosis, senile hyperkeratosis, keratoma senile, and keratosis senilis. The actinic keratosis is a skin-colored to reddish brown or yellowish black ill-defined round or irregularly shaped macule or papule with a dry firmly adherent scale. It is usually 1-3 mm in diameter, but varies up to several centimeters, and can be seen on sun-exposed body regions in persons with many years of solar exposure.
Since the actinic keratosis is the most common precancerous skin lesion, there is an existing demand for a method that is efficient in the treatment of the pathological lesions of the skin to avoid the formation of more severe forms e.g. actinic keratosis. As a matter of fact, with the excepton of new-born babies, parts of the skin surface of nearly everybody have been exposed to the UV radiation of sunlight for a shorter or longer time, consequently, some sorts of pathological lesions of the skin develop when a higher age is reached.
The hydroximic acid derivatives of Formula I below are known from Hungarian Patent No. 177 578 and its equivalent U.S. Pat. No. 4,308,399. The known compounds are suitable for the treatment of diabetic angiopathy.